A means for maintaining an indentation of the ocular coats is desirable in many ophthalmic surgical situations. For example, there is need in vitreous surgery (vitrectomy) to tangentially indent the eye wall to access removal of the peripheral vitreous. In cataract surgery, there is a need or desire to soften the eye prior to incision to reduce the risk of unexpected vitreous loss or expulsive hemorrhage. Further, as well documented in the art, it is desirable to create a scleral depression beneath a peripheral retinal break in a detached retina during a reattachment procedure.
More specifically, the retina is a light sensitive tissue covering the internal surface of the posterior ocular coats. It immediately overlies the retinal pigment epithelium and choroid which are responsible for providing nutrient exchange and temperature regulation to the retina. The retina itself contains light and color sensitive elements termed rods and cones which transmit this information to the brain via interconnecting neural elements including the optic nerve. In the brain, as well as in the retina to a lesser extent, the visual information which has been converted to electrochemical information is further processed and integrated resulting in the phenomenon of sight. Any structural or functional abnormality in this system, whether it be in the light refracting surfaces proximal to the retina, the retina itself, the optic nerve, or the visual centers of the brain may cause vision loss or blindness.
The retina is the most critical element in the circuitry since it contains the light sensitive elements (rods and cones). This process termed phototransduction comes about when light energy (photons) are absorbed by a photoactive chemical in the outer portions of the rods and cones which then undergoes a chemical conformational change. This results in the generation of an electrical current which is propagated along the neural portions of the retina to the optic nerve and subsequently to the visual centers of the brain. In order for this light-bleached photoactive chemical to be regenerated to a form capable of receiving further light information, it must receive nutrients including critical products of vitamin A metabolism from the pigment epithelium to which it is normally intimately apposed (1).
The apposition between the retinal pigment epithelium (RPE) and the photoreceptors can be lost as a result of several different pathologic disease processes. Under normal circumstances, the adhesion between the RPE and retina is tenuously maintained by various active metabolic pumps and other concentration gradients including osmotic and oncotic pressure. These depend upon the health and vitality of the individual. Certain diseases or drugs may interfere with the viability of these pumps and result in separation or detachment of the retina from the pigment epithelium. The above pathologic process is termed exudative retinal detachment and is sometimes amenable to medical therapy.
In other pathologic instances, a full-thickness defect may develop in the retina, as a result of tractional or atrophic forces within the eye. The fluid portion of the vitreous humor may then travel through the defect toward a hole or tear in the retina and insinuate itself in the potential space between the retina and the pigment epithelium. This is termed rhegmatogenous retinal detachment.
In some instances, this amount of fluid and consequent separation may be quite large and result in total detachment of the retina. Because the retinal photoreceptors are no longer apposed to the pigment epithelium, the visual pigments can no longer be regenerated; the exchange of nutrients between the choroid and outer retina is disrupted, and vision is lost. If the retina can be subsequently and permanently reposed to the pigment epithelium, vision can be restored to a variable degree depending upon the criticality of portions of the retina initially detached and the duration of that detachment (2).
Although the association between retinal detachment and blindness has been established for several centuries, the identification of the retinal hole as the etiologic agent in rhegmatogenous retinal detachment and a method of therapy was first documented by Jules Gonin, a Swiss ophthalmologist in the 1930's (3). Since that time a variety of methods, all dependent upon identification and closure of retinal holes have been described for repair of retinal detachment. Gonin first described the necessity of puncture of the sclera to release subretinal fluid and, thereby, permit re-approximation of the retina to the pigment epithelium. Thermal irritation of the RPE and retina through the ocular coats in the vicinity of the retinal tear was employed to seal the edges of the hole or tear and, thereby, prevent fluid movement again through it from the vitreous.
Subsequent investigators reported on the utility of indenting the ocular coats of the eye with a prosthesis sutured within or on the scleral coats as a means of enhancing closure of the retinal tear. This reduced the possibility of re-accumulation of subretinal fluid in the immediate postoperative period. These prostheses have been composed of various absorbable and nonabsorbable materials and were commonly refereed to as scleral implants or explants, depending upon whether they were applied within, or on the scleral coats respectively. They yield generally comparable surgical results. Custodis first made the observation that if the surgeon produced a sufficiently high scleral indentation beneath the retinal hole, the subretinal fluid would resorb after variable periods of time without need for scleral puncture and manual drainage (4). This phenomenon of spontaneous reabsorption of subretinal fluid is ascribed to the effect of the metabolic and other pumping forces in the pigment epithelium and choroid. As a result of this observation, newer techniques of retinal reattachment have evolved in recent years which rely upon auto-reabsorption of subretinal fluid following retinal hole closure (5).
One technique involves the injection of a small volume of expandable inert gas into the vitreous cavity. This bubble upon reaching a larger size through exchange with soluble blood gases, temporarily seals the retinal hole from the inside (vitreal) surface rather than outside (pigment epithelial) surface. The net (temporary) effect is the same in that the vitreal fluid is prevented from travelling through the retinal break into the subretinal space during the time that the bubble is apposed to the break provided that the surface area of the bubble is greater than the surface area of the break. During this time, the normal pumping mechanism evacuates the subretinal fluid and re-apposes the retina to the pigment epithelium. A chorioretinal adhesion is created by thermal means, either prior to the gas injection or subsequent to retinal flattening to prevent subsequent fluid movement through the hole (6). During the time required for the chorioretinal adhesion to mature, the patient's head must be positioned in such a way the bubble is continuously or near continuously apposed to the tear. This technique is effective in between approximately 40 and 70% of instances depending upon the clinical circumstances. Complications reported include failure to reattach the retina, development of new tears, intraocular bleeding, infection, extension of retinal detachment, intraocular scarring, intraocular pressure elevation, and subretinal migration of gas. It is thought to be less effective in eyes that have multiple retinal tears, eyes with retinal tears in the inferior quadrants, near-sighted (myopic) eyes, and eyes that have previously undergone cataract operations.
Another recently developed technique that relies upon the patient's ability to reabsorb subretinal fluid following closure of the retinal hole is the Lincoff balloon buckle as disclosed in U.S. Pat. No. 4,299,277 to Lincoff, issued Nov. 10, 1981. In this technique, a linear catheter with an inflatable tip, analogous to a Foley catheter is introduced into the episcleral space beneath the retinal tear through a conjunctival incision. The catheter is then inflated with saline, producing a localized indentation or buckling of the sclera beneath the break (7). If the indentation is sufficient to close the retinal tear or on its external surface (RPE), the subretinal fluid resorbs and a thermal chorioretinal adhesion is induced either prior to catheter placement, or subsequent to reabsorption by cryo therapy or laser photocoagulation, respectively. While also effective in selected cases, this technique also has limitations including patients who have multiple tears. The potential complications include failure to reattach the retina, bleeding, infection, ocular scarring, and pain. The patient must also wear a catheter taped to the face for a period of time postoperatively with attendant risks of infection, bleeding, slippage or discomfort.
While both of these techniques have gained some acceptance, both are not generally applicable to all eyes with retinal detachment especially those containing more than two retinal tears. Since the average detached retina contains approximately three retinal tears and many have preexisting conditions including cataract surgery, glaucoma, myopia or other complicating circumstances, the application of both of these techniques remains limited.
Based upon these considerations as well as concerns regarding the effectiveness and potential complications, conventional scleral buckling remains the procedure of choice for retinal reattachment repair in most centers in the United States today. Based upon incidence estimates of approximately 1:10,000 persons in the United States developing a retinal detachment per year, it is thought that more than 25,000 Americans undergo retinal reattachment repair annually. Taking into account other causes of retinal detachment, re-operations, subclinical retinal detachments which may not undergo scleral buckling and other circumstances, the procedure may be applicable to as many as 50,000 persons per year.